The recombination system which catalyzes the integration of bacteriophage Mu is most unusual, since it recognizes specific attachment sites on the phage chromosome and recombines them with an apparently random sequence on the host chromosome. The goal of this research program is to elucidate the mechanism by which this integration occurs. We will approach this problem by isolating integration deficient mutants of Mu using techniques which will allow the isolation of both plaque-forming and conditional lethal types of mutants. The defectiveness of the mutants will be confirmed by testing them in several ways for their ability to lysogenize and integrate and by measuring the effect of the mutations on excision. The defect in the mutants will be characterized by determining their ability to be complemented for lysogenization by an int plus phage by analyzing the prophage content and structure of the complemented lysogens. The number of different functions defective in the mutants will be tested by assaying the ability of the mutants to complement each other. The mutants will also be examined biochemically to determine the effect of the mutations on total DNA synthesis and on the DNA forms present in the cell after infection. We will also continue a genetic and biochemical analysis of the host deletions associated with some integrated Mu prophages in an attempt to learn more about this type of Mu-induced mutation, its relation to normal Mu integration, and the factors which affect both types of integration.